arthritis ppt priya
TRANSCRIPT
Submitted to-:
Pranaywal Sir
Submitted by-:
Priya Katiyar
M.Pharm
IInd sem
What is rheumatic arthritis?
When immune system of body mistakenly attacks on lining tissue (synovium) ofjoint, joint become inflammed results over prodution of joint fluid (synovialfluid)and cause permanent joint distruction
auto immune disease
progressive/chronic disease
affect in symmetrical pattern
affect people of all age
cause permanent distruction of joint
affect both male and female
Etiology
RA is caused by combination of genetic and environmental factor that trigger an
abnormal immune response
Possible cause -
Genetic factor- Certain genes that play a role in the immune system are
associated with RA development
Environmental factor- certain infectious agents, such as some viruses
or bacteria may increase suseptibility to RA
Other factor- some hormonal factor may promote RA development in
combination with genetic factors and environmental exposure
Sign and symptoms
Symmetrical joint pain
Swelling of joint
Joint stiffness
Low grade fever
Fatigue
Malaise
redness on joint
Warmth joiny
Loss of fuction
Treatment
The goal of treatment of RA -Relieve pain and inflammation
Prevent joint destruction
Preserve and improve a patient functional activity
Maintain patient normal life
Types of treatment-There are two types of treatment
1)Non pharmacological
2)Pharmacological
Non- pharmacological treatment
weight loose
Occupational therapy
Regular exercise
physiotherapy
healthy diet
Pharmacological Treatment
Traditionally treatment for RA was introduce in a stepwise ‘pyramidal’ manner-
First line drug - such as analgesic and NSAIDS are used
Second line drug - such as Sulfasalazine
Third line drug- such as Azathioprine
Note-
First line drugs are used to relieve pain and second or third line drugs are used
when symptoms are adequately not controlled.
NSAID act by direct inhibition of COX-1 and COX-2 by blocking COX
enzyme site. Cyclo-oxygenase converts the fatty acid arachidonic into
prostaglandin which cause inflammation.
Ex- Aspirin ( dose – 4 to 6 gm/day)
Ibuprofen ( dose – 400 to 600 mg/day)
Side Effect-
GIT complication like ulcer.
GI toxicity.
Intolerence like Dyspepsia.
NSAID (Non-steroidal anti-inflammatory drug)
Preventive therapies for side effect of NSAID
Misoprostol - which is a synthetic prostaglandin effective in prevention of
NSAID induced ulcer by enhancing mucus secretion
Omeprazole - It is also effective in the prevention of NSAID induced GI
complication .It is more effective than misoprostol in maintaining remission
Ranitidine – H 2 receptor antagonist used in the prevention of NSAID
induced GI toxicity
DMARD(Disease modifying anti-rheumatic drug)
Have a major role in managing rheumatic arthritis
Have very different mechanism of action and chemical structure
Has been shown to slow progression of disease
Choice of these drugs depend upon the balance between adverse effect and efficacy
Slow onset of action
Response to treatment usually expected within 4- 6 month
Ex- Methotrexate , Sulfasalazine , Cyclosporin , Azathioprine , Leflunomide etc.
SULFASALAZINE
Most commonly prescribed DMARD due to its favourable risk- benefit ratio
Has high continuation rate.
Low rate of serious adverse effect.
Has been shown to disease progression slow.
Dose- initially 500mg once daily
increasing in weekly steps of 500 mg to 1gm twice daily.
Side effect- Nausea , rashes, marrow suppression, reversible male infertility.
To reduce side effect of nausea the dose is usually titrated from 500 mg to 1gm twice daily .
METHOTREXATE
Used in first line drug therapy
Most effective DMARD
Has a high 5 year continuation rate.
And a low incidence of adverse effect at low weekly dose.
Rapid onset of action of 4-6 weeks.
Easy to administer as a single weekly dose
High response rate of 40-50 %.
Dose- 5-25 mg once weekly.
Side effect - hepatic fibrosis, liver toxicity, stomatitis.
To reduce nausea and stomatitis,folic acid is added to methotrexate therapy.
Steroid
Mainly corticosteroid is used
Suppress cytokines and produce a rapid improvement in sign and symptoms of disease.
Potent anti inflammatory effect, inc mobility and reduce deformity of joint.
Ex- Prednisolone, methyl prednisolone acetate.
Oral prednisolone is used to provide temporary relief until a DMARDS become effective.
Dose- 40 mg for large joint at interval of 1-5 weeks.
( dose depend upon joint size)
Side effect- prophylaxis and osteoporosis.
To reduce side effect- calcium supplement is used with this therapy..
LEFLUNOMIDE-New oral DMARD for RA treatment, isoxazole derivative
Has both anti inflammatory and immuno modulatory properties
Act by inhibiting the synthesis of DNA and RNA in immuno response cell particularly T-cell
Also inhibit the production of cytokines
Rapid on set of action
Side effect- GIT disturbance, alopecia ,hypertension
Dose- 100 mg given once a week ( up to 3 weeks)
To reduce side effect- avoide alcohal, not use in pregnant lady, reduce salt absorption
TNF-alfa inhibitor
It is also a inflammatory mediator that contributes to the pathogenesis of
synovitis and joint destruction substance produced by our body.
These inhibitor can help reduce pain ,stiffness and tender or swollen joint
Ex- Etanercept
is a recombinant human soluble TNF receptor
mechanism of action is competitive inhibition of TNF , binding to cell
surface receptor and prevent TNF mediate cellular response
given subcutaneously
Dose – 4-6 mg/kg( every week)
Side effect- injection site reaction , rhinitis